As discussed in a previous article, the prevailing weight loss method has been the calories in minus calories out equals weight loss or gain model for decades. This simplistic fallacious theory leads one to believe that to be successful at losing weight, all one must do is cut the number of calories consumed and move more. However, millions and millions of dieters and research have shown this method only leads to a bitter reality of failure. The human body is much more complicated to apply a simple math equation for losing weight.
Weight gain is a hormone problem, not a calorie problem. Not to say that calories don’t matter; however, the body is extremely sensitive to a reduction in calories. A drop in calories always has an equal decrease in caloric expenditure (metabolism), resulting in yo-yo dieting. The good news is that one can control the hormone responsible for fat storage to lose body fat and keep it off.
Insulin is referred to by scientists as the fat-storage hormone and is the only hormone that can store food as fat. There is a delicate balance between the amount of insulin one’s pancreas secretes in response to the amount of food one eats, namely carbohydrates. It is well documented consuming carbohydrates is the most significant factor in glycemia (blood glucose) and that restricting carbohydrates results in the highest reduction in overall blood glucose levels and weight loss (Feinman et al., 2015; Russell-Jones et al., 2007).
As one eats carbohydrates, the body breaks them down into a simple more absorbable sugar called glucose. Glucose is transported through the intestinal lining and is dissolved in the blood, traveling freely around the body, ready to be used. As your blood glucose levels rise, this signals the pancreas to release insulin, and insulin governs glucose processing.
Glucose is processed by insulin in two different ways. As glucose levels rise, insulin converts a portion of it to glycogen, stored in muscle cells and the liver. Once all the storage space is taken up, and it doesn’t take much, especially if you don’t exercise, insulin will convert the rest to triglycerides and store it as adipose tissue, FAT. Insulin is a facilitator of lipogenesis or fat storage and a deterrent to lipolysis or the breaking down of fat for energy. Even low levels of circulating insulin have been shown to prevent the breakdown of fat to be used as energy.
Obesity has long been associated with higher insulin levels (Ferrannini et al., 1997; Kahn et al., 2000; Polonski et al., 1988; Russell-Jones et al., 2007). Obese individuals secrete much higher levels of insulin in response to the food they eat than people of normal weight. Moreover, insulin levels remain elevated in obese individuals after a meal, but they rapidly return to baseline in lean people.
The "higher insulin levels cause weight gain" hypothesis is effortlessly tested. Administering insulin to a number of subjects then measuring their weight gain can establish a causal relationship. The question is: If somebody takes exogenous insulin, will they gain fat? The answer is a resounding yes. Patients who use insulin regularly and the doctors who prescribe it have firsthand knowledge of this ugly truth. The higher one's insulin, the more fat a person accumulates.
The question of how insulin causes weight gain is a highly complex problem, in which researchers haven't found all the answers. But there are many theories. One theory states that higher insulin levels inhibit leptin from doing its job to signal satiety. In lean individuals, leptin levels rise in response to a meal causing a feeling of satiety and then dropping back to baseline. However, in obese individuals, higher leptin levels do not signal satiety and remain at higher concentrations after meals causing one to remain feeling hungry.
Fasting insulin and fasting leptin levels are increased in obese individuals, demonstrating both insulin and leptin resistance (Baskin, D. G., et al. 1999; Lustig, R. H., et al. 2004; Mangi, P. et al. 2005). However, leptin resistance does not directly lead to weight gain. As one becomes insulin resistant and gains weight, they become leptin resistant. Higher insulin levels are the foundation of one's metabolic dysfunction, and as one controls their insulin levels, leptin also starts to function correctly.
As one starts to understand insulin's role in the body, one sees how absurd it is to discuss weight loss without mentioning insulin. The critical point is not how insulin causes obesity, but that higher insulin levels do cause obesity.
Dietary Practice Pearls:
Avoiding food is the most effective way to reduce insulin levels and improve insulin sensitivity.
Start intermittent fasting 12 or more hours per day.
Carbohydrate restriction has the greatest effect on lowering blood glucose levels and insulin resistance.
Studies show that carbohydrate restriction has the biggest benefit for losing weight.
Replace carbohydrates with protein and vegetables.
Only use protein sources that are wild, pastured, and grass-fed and finished.
Only consume vegetables that are organic. If organic vegetables aren’t available, do not eat them.
Do not consume polyunsaturated vegetable oils like corn oil, soy oil, sunflower oil, and safflower oil.
Consume avocado oil, olive oil, coconut oil, beef tallow, lard, and butter. They are your best friends.
Recommended Supplements to optimize insulin, blood glucose, and control weight gain.
Michael Furci is a Family Nurse Practitioner at Tenpenny Integrative Medical Center. To make an appointment call (440)239-3438
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Feinman, R. D., Pogozelski, W. K., Astrup, A., Bernstein, R. K., Fine, E. J., Westman E. C., . . . Worm, N. (2015). Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base. Nutrition, 31(1), 1-13. https://doi.org/10.1016/j.nut.2014.06.011
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Volek, J. S., Fernandez, M. L., Feinman, R. D., & Phinney, S. D. (2008). Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Progress in Lipid Research, 47(5),307-318. DOI: 10.1016/j.plipres.2008.02.003